A report published in the May 10, 2006 issue of the Journal of Neuroscience ( http://www.jneurosci.org/ ) concluded that oxidative damage to the mitochondria of the brain's cells from internal processes could be one of the main causes of Parkinson's disease (PD). Mitochondria are organelles within the cells that are responsible for generating energy.

Neuroscientists at the University of Virginia Health System compared the brains of ten deceased Parkinson's patients to those of twelve normal individuals matched for age. The diseased brains were found to have 50 percent more damage from oxygen free radicals to a mitochondrial protein structure known as complex I, which is the first stop in the electron transport chain that produces an electrical charged used to make energy. Lead researcher Dr Jim Bennett, who is neurologist at the University of Virginia, stated, "This part of the protein complex is being damaged by oxygen free radicals more in a brain with Parkinson's than it is in someone of same age who does not have PD. If this damage is caught in people early on, we might interrupt the progression of Parkinson's disease. Such treatment is hypothetical at this point, but it is rational."

At this point, Dr Bennett's team does not yet know why complex 1 is damaged in Parkinson's disease patients. "It could be that something has gone terribly wrong with the mitochondrial genome passed down by a person's mother that codes for several proteins in complex I," he suggested. "Something could be wrong in the coding for genes that help complex I assemble. Or there could be environmental toxins. Our research is a first real step in understanding at a detailed biochemical level what the challenge is."